Journal of Vestibular Research 25 (2015) 105117 105

DOI 10.3233/VES-150553
IOS Press

Benign paroxysmal positional vertigo:

Diagnostic criteria
Consensus document of the Committee for the Classification of Vestibular Disorders of the Brny
Society

Michael von Breverna,, Pierre Bertholonb , Thomas Brandtc , Terry Fifed , Takao Imaie ,
Daniele Nutif and David Newman-Tokerg
a
Department of Neurology, Park-Klinik Weissensee, Berlin, Germany
b
Department of Otolaryngology Head and Neck Surgery, Bellvue Hospital, Saint-Etienne, France
c
Institute of Clinical Neuroscience, Ludwig-Maximilian University, Munich, Germany
d
Barrow Neurological Institute, University of Arizona College of Medicine, Phoenix, AZ, USA
e
Department of Otolaryngology Head and Neck Surgery, Osaka University Graduate School of Medicine, Japan
f
Department of Otolaryngology Head and Neck Surgery, University of Siena, Italy
g
Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MA, USA

Received 2 May 2014

Accepted 3 June 2015

Abstract. This article presents operational diagnostic criteria for benign paroxysmal positional vertigo (BPPV), formulated by
the Committee for Classification of Vestibular Disorders of the Brny Society. The classification reflects current knowledge of
clinical aspects and pathomechanisms of BPPV and includes both established and emerging syndromes of BPPV. It is anticipated
that growing understanding of the disease will lead to further development of this classification.

Keywords: Vertigo, positional, nystagmus, diagnosis, criteria

1. Introduction lar symptoms [13]. Individual subcommittees includ-

The following diagnostic criteria for benign parox-
ysmal positional vertigo (BPPV) are part of the Inter-
national Classification of Vestibular Disorders (ICVD)
an endeavour for classification of vestibular disorders
steered by the Committee for Classification of Vestibu-
lar Disorders of the Brny Society. As a first step and
prerequisite for the classification of vestibular disor-
ders, the Classification Committee of the Brny Soci-
ety published a consensus on the definition of vestibu-
Corresponding author: Michael von Brevern, Department of
Neurology, Park-Klinik Weissensee, Schnstrasse 80, 13086 Berlin,
Germany. Tel.: +49 30 96283700; Fax.: +49 30 96283705; E-mail:
von.brevern@park-klinik.com.
ing otolaryngologists and neurologists from at least
three continents have been tasked with defining con-
sensus diagnostic criteria for specific vestibular disor-
ders.
We have taken additional steps to ensure the broad-
est possible consensus for the criteria. The classifica-
tion has been presented and discussed at two meet-
ings of the Brny Society in 2010 and 2012. Fur-
thermore, a draft of the classification was presented
to five other medical societies engaged in neurotology
(American Academy of Otolaryngology Head and
Neck Surgery, American Neurotology Society, Amer-
ican Otological Society, European Academy of Otol-
ogy and Neuro-Otology, and Japan Society of Equilib-
rium Research). The members of the Brny-Society
were invited to comment on the last draft of this clas-

ISSN 0957-4271/15/$35.00 
c 2015 IOS Press and the authors. All rights reserved
106 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria
sification before publication by means of an online
internal review system. Comments from Brny So-
ciety members and from the consulted medical so-
cieties were discussed and, where appropriate, incor-
porated by the subcommittee before the final version
of this classification was approved. Finally, we have
taken steps to ensure that our document is harmonious
with current published therapeutic guidelines from the
American Academy of Neurology [31] and the Amer-
ican Academy of Otolaryngology Head and Neck
Surgery [11].
The format of this classification is modelled on the
International Classification of Headache Disorders. It
includes both established syndromes (Sections 2.1 to
2.4) and emerging and controversial syndromes (Sec-
tions 3.1 to 3.4). The operational criteria are supported
by notes and comments.
1.1. Terminology
Because symptoms are triggered by the act of mov-
ing the head to a new position, rather than by maintain-
ing the head in a particular posture or position, some
authors have advocated for the use of the term po-
sitioning vertigo rather than positional vertigo for
BPPV. A similar issue arises in distinguishing posi-
tioning nystagmus from positional nystagmus on
the basis of whether the finding is transient after head
positioning. While these distinctions make mechanis-
tic sense and may be of diagnostic value, it was the
groups judgment that current usage of the term po-
sitional in BPPV or to describe its associated nystag-
mus is too ubiquitous to change clinical practice. Thus,
the term positional is preserved in the definitions be-
low and positioning is not used.
1.2. Epidemiology
BPPV is the most frequent vestibular disorder:
its cumulative incidence in the general population
amounts during lifetime to 10% [79]. The time course
of BPPV is characterised by spontaneous remissions
that occur typically after days to weeks [41] and re-
currences that occur in about 50% of patients [61]. Al-
though BPPV is usually self-limiting, it inflicts a con-
siderable personal and socio-economic burden [55,79].
1.3. Pathophysiology
According to a widely accepted theory BPPV is
usually caused by otoconia that are dislodged from the
otolith macula beds and are trapped in a semicircular
canal. Gravity causes them to move after changes of
the head position in the plane of the affected canal. The
resulting inappropriate endolymph flow deflects the
cupula and thus modulates the activity of the vestibu-
lar afferents of the affected canal, causing attacks of
positional vertigo and nystagmus (canalolithiasis) [15].
Less common, BPPV can be attributed to otoconia that
are attached to the cupula of a semicircular canal and
render it sensitive to gravity (cupulolithiasis) [5,51,73].
The development of pathophysiological concepts of
BPPV that aimed to understand the clinical features
of the disease as a mechanical irritation of a semicir-
cular canal has been an intellectual challenge [15,50].
Schuknecht coined the term cupulolithiasis on the ba-
sis of histological studies of the temporal bones from
patients with BPPV [67]. Incidentally, he also has pro-
vided a documentation of canalolithiasis, although he
did not recognize the pathophysiological meaning of
this finding [67].
The critical role of the receptors of the semicir-
cular canals is supported by the direction of posi-
tional nystagmus in BPPV reflecting the known exci-
tatory and inhibitory connections of the canal recep-
tors with specific extraocular eye muscles [2]. The hy-
pothesis of canalolithiasis and cupulolithiasis is sup-
ported by in-vitro and in-vivo animal models [63,71],
by mathematical models [33,40,65] and by the effi-
cacy of specific canal clearing procedures [31,32,54]
and plugging of the affected semicircular canal [10].
Furthermore, particulate matter within the posterior
canal has been observed intraoperatively in patients
with BPPV [64,80]. This debris has been examined by
scanning electron microscopy and appeared morpho-
logically consistent with degenerated otoconia [80]. Of
note, particulate matter has also been found in the pos-
terior semicircular canal of subjects without a history
of BPPV [49,59]. This finding is not contradictory to
the pathophysiology of BPPV as discussed above as
physio-mathematical models have shown that the pre-
requisite for BPPV is a certain amount of otoconia
within the affected semicircular canal reaching a crit-
ical mass and that an agglomeration of these particles
promotes the hydrodynamic effect of otoconia moving
in the canal [33,40].
There are open questions that need to be addressed
in the future. It has been postulated that loose otoco-
nia within the short arm of the semicircular canals (on
the utricular side of the cupula) may also cause posi-
tional vertigo [17,18]. Furthermore, canalolithiasis and
cupulolithiasis are not mutually exclusive and may co-
 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria
exist simultaneously in the same semicircular canal but
such a combination has not been documented with eye
movement recording so far.
There are clinical findings that are possibly associ-
ated with BPPV but not yet sufficiently understood.
Spontaneous nystagmus not provoked by positioning is
not a core feature of BPPV, although pseudosponta-
neous nystagmus is typical of horizontal canal BPPV
(see comment to 1.3 further below). Rarely, however,
spontaneous nystagmus beating in a direction that cor-
responds to the stimulation of a single semicircular
canal irrespective of head position has been observed
in patients that otherwise fulfilled diagnostic criteria
for canalolithiasis or cupulolithiasis. This finding is
usually brief, rarely lasting longer than a few minutes
and has been described as a complication of positional
therapy and after shaking the head in the plane of the
canal affected by canalolithiasis [28,76] and may pos-
sibly also occur spontaneously [58]. The pathophys-
iology is unclear. A canalith jam implying a lock-
ing of the cupula in a fixed position by canalith de-
bris, either directly jamming the cupula or indirectly
blocking endolymph flow in the canal has been postu-
lated [28,58,76].
Finally, patients with persistent geotropic direction-
changing positional nystagmus in the supine lateral
head positions in the absence of central neurologic
signs and with normal results in cerebral imaging have
been described [37,44]. This type of nystagmus is nei-
ther compatible with mobile otoconia in a semicircu-
lar canal nor with dense otoconia attached to a cupula.
However, there seems to be an association between
persistent geotropic direction-changing positional nys-
tagmus and canalolithiasis and cupulolithiasis, as some
of these patients have developed classical variants of
BPPV at follow-up [37,44]. It has been suggested that
this phenomenon may be due to changes of the den-
sity of the cupula or the endolymph [37,44], but this
remains speculative.
1.4. Diagnosis
The complete diagnosis includes the specification of
the affected semicircular canal(s) and the pathophysi-
ology (canalolithiasis or cupulolithiasis). The definite
diagnosis of BPPV requires diagnostic positional ma-
neuvers that lead to the observation of a canal-specific
positional nystagmus. Clinical features essential for
the diagnosis are the latency, direction, time course,
and duration of positional nystagmus. Usually, further
vestibular and auditory testing is indicated only when
107
a pre-existing disorder of the inner ear (e.g. vestibu-
lar neuritis, Menires disease) is suspected. Similarly,
brain or ear imaging is not required in typical cases of
BPPV [11].
Positional testing involves the provocation of ver-
tigo and nystagmus, and different maneuvers test dif-
ferent semicircular canals. A canal-specific response
is diagnosed when a rotation of the head in the plane
of a semicircular canal evokes positional nystagmus of
maximal intensity (in terms of slow phase velocity).
As a rule (and in contrast to central positional nystag-
mus), positional nystagmus in BPPV always beats in
the plane of the affected canal and in the expected di-
rection for canal excitation or inhibition [19].
Basically, the head is brought first into such a po-
sition that the affected semicircular canal is spatially
vertical and thus aligned with gravity. In a second step,
the head is then rotated in the plane of the affected
canal. In the Dix-Hallpike maneuver, the head of the
sitting patient is turned 45 toward the side to be tested
and then laid back quickly into a head-hanging posi-
tion [27]. In the side-lying maneuver (Semont diagnos-
tic maneuver) the sitting patient is tilted quickly to the
side to be tested with the head turned 45 to the oppo-
site side [24]. It is noted that both maneuvers not only
test for lithiasis of the posterior canal of one side but
also for the anterior canal of both sides [2,6,16]. For
testing of the horizontal canal, the supine roll test is
used: the head of the patient in the supine position is el-
evated about 30 and then turned quickly to either side.
It is essential to perform positional maneuvers for both
the vertical and the horizontal semicircular canals in
every patient with positional vertigo as multiple canals
may be affected [8,60].
For observation of positional nystagmus, Frenzel
goggles or video-oculography can be helpful, partic-
ularly when the nystagmus is weak or momentary.
Recording of eye movements may enhance ones abil-
ity to observe and to classify nystagmus in canalolithi-
asis of the anterior canal (3.1), in cupulolithiasis of
the posterior canal (3.2), in lithiasis of multiple canals
(3.3.) and in possible BPPV (3.4). In most cases, how-
ever, nystagmus can be seen clinically without spe-
cial equipment. The direction of nystagmus is essen-
tial to specify the affected canal. Indeed, the posterior
canal is by far the most frequently affected canal (80
90%); next is the horizontal canal (530%) [25,38,73].
Involvement of the anterior canal is rare, account-
ing for only 1% to 2% of patients in large case se-
ries [38,60,81] although some recent reports have sug-
gested a considerably higher incidence [20,45]. Theo-
108 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria
retically, each of the three semicircular canals of the
labyrinth can be affected by canalolithiasis or cupu-
lolithiasis, resulting in six combinations (not counting
multiple canal involvement) for each ear. Except for
cupulolithiasis of the anterior canal, all these combina-
tions have been documented by eye movement record-
ings and are included in this classification.
Therapeutic positional maneuvers are highly effec-
tive for treatment of BPPV, particularly when canaloli-
thiasis is present [11,31]. Thus, if positional nystag-
mus disappears immediately after positional therapy,
this strongly supports the diagnosis of BPPV. Such a
favourable response to treatment is not mandatory for
the diagnosis, and patients refractory to treatment do
occur. However, repeated lack of response to therapy
should generally prompt consideration of alternative
diagnoses that may mimic BPPV closely [11].
The differential diagnosis of BPPV includes cen-
tral positional vertigo due to vestibular migraine [77]
and structural brainstem and cerebellar lesions, typi-
cally in the vicinity of the fourth ventricle [14]. CNS
disease can usually be excluded by a thorough neuro-
logical examination, but some cases may be challeng-
ing to diagnose [48]. Greater care should be taken in
patients with dominantly horizontal or downbeat po-
sitional nystagmus forms, since these are most fre-
quently reported in central mimics [9,46,48]. Cere-
bral imaging with MRI is usually only indicated when
symptoms or signs of concurrent brainstem or cerebel-
lar dysfunction are present, or when positional vertigo
and nystagmus present with atypical features or fail
to resolve with repeated therapeutic positional maneu-
vers [11].
2. Diagnostic criteria for benign paroxysmal
positional vertigo
Previously used terms: benign paroxysmal position-
ing vertigo, benign positional vertigo, paroxysmal po-
sitional vertigo, vestibular lithiasis.
2.1. Canalolithiasis of the posterior canal (pc-BPPV)
A. Recurrent attacks1 of positional vertigo or posi-
tional dizziness2,3,4 provoked by lying down or
turning over in the supine position5 .
B. Duration of attacks < 1 min6 .
C. Positional nystagmus7 elicited after a latency of
one or few seconds8 by the Dix-Hallpike maneu-
ver or side-lying maneuver (Semont diagnostic
maneuver). The nystagmus is a combination of
torsional nystagmus with the upper pole of the
eyes beating toward the lower ear combined with
vertical nystagmus9 beating upward (toward the
forehead) typically lasting < 1 minute10,11,12,13 .
D. Not attributable to another disorder14.
Notes
1. In addition to attacks of positional vertigo, pati-
ents may have prolonged mild unsteadiness [26],
even after successful treatment of benign parox-
ysmal positional vertigo [66].
2. BPPV typically leads to positional vertigo but oc-
casionally patients may complain of positional
dizziness.
3. Other complaints during the attacks include ex-
ternal vertigo (the visual sense of environmen-
tal motion that often accompanies the internal
vestibular sense) [13], unsteadiness, and vege-
tative symptoms such as nausea, sweating, and
tachycardia.
4. Positional vertigo or dizziness must be distin-
guished from orthostatic symptoms present only
on arising but not with other positional trig-
gers [13].
5. Attacks may not only be provoked in bed but also
by other head movements (e.g., tilting the head
backward [i.e., chin upward] or forward).
6. Patients may overestimate the duration of single
attacks and mild, residual symptoms after an at-
tack occasionally last minutes or hours. Further-
more, attacks may be triggered repetitively, caus-
ing more extended symptoms. The duration of
vertigo should not, however, generally exceed 1
minute; single attacks lasting consistently longer
should be considered atypical and spark consid-
eration of alternate or additional diagnoses.
7. If positional nystagmus disappears immediately
after positional therapy, this further supports the
diagnosis.
8. The latency between the completion of the diag-
nostic positional maneuver and the onset of po-
sitional nystagmus may be as long as 40 seconds
in rare cases [3].
9. The torsional component of positional nystag-
mus is slightly more prominent in the lower eye,
 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria
whereas the vertical component is slightly more
prominent in the upper eye [39]. If fixation is
not suppressed, the nystagmus may appear dom-
inantly torsional, since fixations ability to sup-
press torsional eye movements is limited relative
to suppression for vertical movements. The di-
rection of the patients gaze may influence the
appearance of positional nystagmus. If gaze is
directed to the lower ear, nystagmus may ap-
pear predominately torsional; if directed to the
upper ear, it may appear predominantly verti-
cal [14]. Independent of orbital eye position, the
eye movement in a head-referenced coordinate
system remains fixed in the plane of the posterior
semicircular canal.
10. Usually, the duration of positional nystagmus
does not exceed 40 seconds before it damps spon-
taneously [3].
11. Typically, positional nystagmus increases rapidly
in intensity and then declines more slowly (cre-
scendo-decrescendo) [3].
12. Nystagmus of lower intensity with reversed di-
rection may appear after the initial positional
nystagmus has ceased [3].
13. After the patient returns to the upright position,
positional nystagmus with reversed direction of
lesser intensity and shorter duration often occurs.
Furthermore, fatigability of nystagmus and ver-
tigo with repetitive positional testing is a com-
mon finding.
14. History and physical and neurological examina-
tions do not suggest another vestibular disorder
or such a disorder is considered but ruled out
by appropriate investigations or such disorder
is present as a comorbid condition that can be
clearly differentiated.
Comments
Canalolithiasis of the posterior canal is by far the
most common variant of benign paroxysmal positional
vertigo, accounting for 8090% of cases [60]. The
right labyrinth is affected slightly more often than the
left [78].
The occurrence of a bilateral canalolithiasis of the
posterior canal is not rare, but is more prevalent in post-
traumatic cases than in idiopathic canalolithiasis [47].
Note that unilateral benign paroxysmal positional ver-
tigo may mimic bilateral benign paroxysmal positional
vertigo of the posterior canal if the positional maneu-
109
ver is executed without appropriate alignment of the
head [68].
The occurrence of canalolithiasis of the posterior
canal without positional nystagmus is controversial but
improvement of positional vertigo after a therapeutic
positional maneuver in such patients with a typical his-
tory of benign paroxysmal positional vertigo has been
reported [34,72]. These patients should be coded as
3.4. Possible benign paroxysmal positional vertigo. It
is conceivable that the number of otoconia in the pos-
terior canal is sufficient to evoke subjective symptoms
but insufficient to stimulate the vestibulo-ocular re-
flex [40].
2.2. Canalolithiasis of the horizontal canal
(hc-BPPV)
A. Recurrent attacks1 of positional vertigo or posi-
tional dizziness2,3,4 provoked by lying down or
turning over in the supine position5 .
B. Duration of attacks < 1 min6 .
C. Positional nystagmus7 elicited after a brief la-
tency or no latency8 by the supine roll test, beat-
ing horizontally9 toward the undermost ear10,11
with the head turned to either side (geotropic
direction changing nystagmus) and lasting <
1 min12,13 .
D. Not attributable to another disorder14.
Notes
1. Besides attacks of positional vertigo, patients
may have prolonged mild unsteadiness.
2. BPPV typically leads to positional vertigo but oc-
casionally patients may complain of positional
dizziness.
3. Other complaints during the attacks include ex-
ternal vertigo (the visual sense of environmen-
tal motion that often accompanies the internal
vestibular sense) [13], unsteadiness, and vege-
tative symptoms such as nausea, sweating, and
tachycardia.
4. Positional vertigo or dizziness must be distin-
guished from orthostatic symptoms present only
on arising but not with other positional trig-
gers [13].
5. Attacks may not only be provoked in bed but also
by other head movements (e.g., during rapid lat-
eral head rotations while erect [4], tilting the head
backward [i.e., chin upward] or forward).
110 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria
6. Patients may overestimate the duration of sin-
gle attacks and mild, residual symptoms after an
attack occasionally last minutes or hours. Fur-
thermore, attacks may be triggered repetitively,
causing more extended symptoms. The dura-
tion of vertigo should not, however, generally
exceed 1 minute; single attacks lasting consis-
tently longer should be considered atypical and
spark consideration of alternate or additional di-
agnoses.
7. If positional nystagmus disappears immediately
after positional therapy, this further supports the
diagnosis.
8. The latency between the completion of the diag-
nostic positional maneuver and the onset of posi-
tional nystagmus depends on the acceleration of
the positional change: the higher the acceleration
of the head turn, the shorter the latency and the
higher the intensity of nystagmus [4]. With brisk
positional maneuvers the latency is typically 1 or
2 seconds. Likewise, the intensity of nystagmus
depends on the angle of head rotation: the inten-
sity of nystagmus tends to be higher with larger
head rotations in the head roll test [69].
9. The direction of positional nystagmus is predom-
inantly horizontal with a smaller torsional com-
ponent beating with the upper pole of the eye to
the lower ear [2].
10. Nystagmus of lower intensity with reversed di-
rection may appear after the initial positional
nystagmus has ceased [4].
11. Probably, canalolithiasis of the horizontal canal
may also cause apogeotropic horizontal posi-
tional nystagmus. This would be the case when
otoconia are located in the anterior part of the
horizontal canal (close to the cupula). During
the supine roll test to the healthy ear, otoconia
would then fall toward or onto the cupula, re-
sulting in transient or long-lasting apogeotropic
horizontal positional nystagmus. The supine roll
test to the affected ear would provoke tran-
sient apogeotropic horizontal positional nystag-
mus [30,42,62]. In these patients, transformation
from apogeotropic to geotropic positional nys-
tagmus can be observed during diagnostic posi-
tional maneuvers [21,42,73]. In contrast, persis-
tence of apogeotropic horizontal positional nys-
tagmus following several cycles of the supine roll
test is expected with cupulolithiasis.
12. The duration of nystagmus as documented with
eye movement recording may exceed 1 minute
before it damps spontaneously, however, it does
not exceed 2 minutes [2,25].
13. Typically, positional nystagmus increases rapidly
in intensity and then declines more slowly (cres-
cendo-decrescendo) [4].
14. History and physical and neurological examina-
tions do not suggest another vestibular disorder
or such a disorder is considered but ruled out
by appropriate investigations or such disorder
is present as a comorbid condition that can be
clearly differentiated.
Comments
Several clinical signs may indicate the side of the
affected ear and are confirmatory for the diagnosis.
The intensity of nystagmus is usually stronger with the
head turned to the affected ear in the supine roll test [4].
Note that the net angle and acceleration of the head ro-
tation should be similar for head turns to the right and
left to allow for comparison of nystagmus intensity.
Flexing the head forward in the upright position (with
the face downward) may elicit a transient nystagmus
beating toward the affected ear. Lying backward from
the sitting position may provoke transient nystagmus
beating toward the healthy ear [23].
Besides positional nystagmus, pseudospontaneous
nystagmus (see also comment to 2.3) may also be ob-
served in the upright head position beating either ip-
silesional or contralesional [1,52].
Caloric irrigation of the affected ear [70] and the
head thrust test [35] may reveal horizontal canal pare-
sis (possibly due to partial plugging of the canal) that
is reversible after successful positional therapy [70].
Transition from geotropic to apogeotropic nystag-
mus may occur during diagnostic and therapeutic ma-
neuvers, e.g. when the patient bends over from the sit-
ting to the head-on-knees position [69]. Transition of
canalolithiasis from the posterior canal to the horizon-
tal canal may occur as a result of therapeutic positional
maneuvers [36].
2.3. Cupulolithiasis of the horizontal canal
(hc-BPPV-cu)
A. Recurrent attacks1,2 of positional vertigo or po-
sitional dizziness3,4,5 provoked by lying down or
turning over in the supine position.
 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria
B. Positional nystagmus6 elicited after a brief la-
tency or no latency by the supine roll test, beating
horizontally7 toward the uppermost ear with the
head turned to either side (apogeotropic direction
changing nystagmus), and lasting > 1 minute8 .
C. Not attributable to another disorder9 .
Notes
1. The duration of an attack of positional vertigo is
usually less than 1 minute as patients tend to re-
turn the head into a position where vertigo and
nystagmus cease. However, the duration can be
longer if the head is kept in the provoking posi-
tion. Furthermore, due to the spatial orientation
of the affected cupula, patients may have persist-
ing vertigo or dizziness of lower intensity in the
upright position.
2. Besides attacks of positional vertigo, patients
may have prolonged mild unsteadiness.
3. BPPV typically leads to positional vertigo but oc-
casionally patients may complain of positional
dizziness.
4. Other complaints during the attacks include ex-
ternal vertigo (the visual sense of environmen-
tal motion that often accompanies the internal
vestibular sense) [13], unsteadiness, and vege-
tative symptoms such as nausea, sweating, and
tachycardia.
5. Positional vertigo or dizziness must be distin-
guished from orthostatic symptoms present only
on arising but not with other positional trig-
gers [13].
6. If positional nystagmus disappears immediately
after positional therapy, this further supports the
diagnosis.
7. The direction of positional nystagmus is predom-
inantly horizontal with a smaller torsional com-
ponent beating with the upper pole of the eye to
the upper ear [2].
8. Typically, intensity of positional nystagmus buil-
ds up slowly over approximately 30 seconds and
then gradually decays over a longer period of sev-
eral minutes [2,5].
9. History and physical and neurological exami-
nations do not suggest another vestibular disor-
der or such a disorder is considered but ruled
out by appropriate investigations or such disor-
der is present as a comorbid condition that can
be clearly differentiated. As direction-changing
111
apogeotropic positional nystagmus also occurs
as a sign of central-vestibular dysfunction, it is
mandatory to exclude CNS disease.
Comments
Several clinical signs can indicate the side of the af-
fected ear and are confirmatory for the diagnosis. The
intensity of positional nystagmus is usually stronger
with the head turned away from the affected ear in the
supine roll test. Note that the net angle and acceleration
of the head rotation should be similar for head turns to
the right and left to allow for comparison of nystagmus
intensity.
Besides positional nystagmus, pseudospontaneous
nystagmus may also be observed in the upright head
position beating typically to the affected ear [1,12,52].
Pseudospontaneous nystagmus is a form of positional
nystagmus that happens to occur with the head in the
upright position, making it appear superficially similar
to spontaneous nystagmus. In contrast to spontaneous
nystagmus, pseudospontaneous nystagmus is strongly
influenced by head position and ceases with the head
tilted about 30 forward [12]. Pseudospontaneous nys-
tagmus is attributed to the 30 angle between the plane
of the horizontal canal and the horizontal plane of the
head in the upright position that places the ampulla in
a higher position than the rest of the canal [12]. Grav-
ity causes deflection of the cupula and produces hor-
izontal nystagmus beating to the side of the horizon-
tal canal affected by cupulolithiasis. Flexing the head
90 forward in the upright position may elicit pseu-
dospontaneous nystagmus beating toward the healthy
ear [12,23]. In the supine position a weak persistent
nystagmus beating toward the affected ear may be ob-
served that subsides when the head is turned slightly to
that side [12].
Apogeotropic direction changing positional nys-
tagmus is not synonymous with cupulolithiasis but
may also occur with canalolithiasis of the horizon-
tal canal [30,42,62,74]. Rapid transition from apo-
geotropic to geotropic direction changing positional
nystagmus during the supine roll test may be due
to a variant of canalolithiasis where otoconia are lo-
cated in the anterior part of the horizontal canal (see
canalolithiasis of the horizontal canal). In contrast, per-
sistence of an apogeotropic direction of positional nys-
tagmus with repetitive performance of the supine roll
test is supportive of the diagnosis of cupulolithiasis of
the horizontal canal.
112 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria
2.4. Probable benign paroxysmal positional vertigo,
spontaneously resolved
A. Recurrent attacks1 of positional vertigo or posi-
tional dizziness2,3,4 provoked by lying down or
turning over in the supine position5 .
B. Duration of attacks < 1 min6 .
C. No observable nystagmus and no vertigo with
any positional maneuver.
D. Not attributable to another disorder7 .
Notes
1. Besides attacks of positional vertigo, patients
may have prolonged mild unsteadiness.
2. BPPV typically leads to positional vertigo but oc-
casionally patients may complain of positional
dizziness.
3. Other complaints during the attacks include ex-
ternal vertigo (the visual sense of environmen-
tal motion that often accompanies the internal
vestibular sense) [13], unsteadiness, and vege-
tative symptoms such as nausea, sweating, and
tachycardia.
4. Positional vertigo or dizziness must be distin-
guished from orthostatic symptoms present only
on arising but not with other positional trig-
gers [13].
5. Attacks may not only be provoked in bed but also
by other head movements (e.g., tilting the head
upward [i.e., chin upward] or forward).
6. Patients may overestimate the duration of single
attacks and mild, residual symptoms after an at-
tack occasionally last minutes or hours. Further-
more, attacks may be triggered repetitively, caus-
ing more extended symptoms. The duration of
vertigo should not, however, generally exceed 1
minute; single attacks lasting consistently longer
should be considered atypical and spark consid-
eration of alternate or additional diagnoses.
7. History and physical and neurological examina-
tions do not suggest another vestibular disorder
or such a disorder is considered but ruled out
by appropriate investigations or such disorder
is present as a comorbid condition that can be
clearly differentiated.
Comments
The diagnosis of probable benign paroxysmal posi-
tional vertigo that has resolved spontaneously is made
during the symptom-free interval. As a consequence,
the formerly affected semicircular canal cannot be
identified. A history of temporary, isolated episodic po-
sitional vertigo with appropriate episode duration and
characteristic triggers strongly supports the diagnosis
of probable benign paroxysmal positional vertigo that
has resolved spontaneously.
The differential diagnosis should include vestibu-
lar migraine, which likewise can present with episodic
positional vertigo. In contrast to BPPV, episodes of
positional vertigo in vestibular migraine tend to be
of shorter duration with frequent recurrences, tend to
present at an earlier age, and are often accompanied by
migraine symptoms (headache, photophobia, phono-
phobia, migraine aura) [77].
3. Emerging and controversial syndromes
The following syndromes are rare variants of BPPV
and may be difficult to differentiate from central posi-
tional vertigo.
3.1. Canalolithiasis of the anterior canal1 (ac-BPPV)
A. Recurrent attacks2 of positional vertigo or posi-
tional dizziness3,4,5 provoked by lying down or
turning over in the supine position6 .
B. Duration of attacks < 1 min7 .
C. Positional nystagmus8 elicited immediately or
after a latency of one or few seconds9 by the Dix-
Hallpike maneuver (on one or both sides) or in
the supine straight head-hanging position, beat-
ing predominantly vertically downward10 and
lasting < 1 min.
D. Not attributable to another disorder11.
Notes:
1. The diagnosis of definite canalolithiasis of the
anterior canal (3.1.1) can be made on the basis of
immediate resolution of positional nystagmus af-
ter therapeutic maneuvers. In contrast, probable
canalolithiasis of the anterior canal (3.1.2) can
be diagnosed only after exclusion of CNS disease
when positional nystagmus is refractory to thera-
peutic maneuvers.
2. Besides attacks of positional vertigo, patients
may have prolonged mild unsteadiness.
 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria
3. BPPV typically leads to positional vertigo but oc-
casionally patients may complain of positional
dizziness.
4. Other complaints during the attacks include ex-
ternal vertigo (the visual sense of environmen-
tal motion that often accompanies the internal
vestibular sense) [13], unsteadiness, and vege-
tative symptoms such as nausea, sweating, and
tachycardia.
5. Positional vertigo or dizziness must be distin-
guished from orthostatic symptoms present only
on arising but not with other positional trig-
gers [13].
6. Attacks may not only be provoked in bed but also
by other head movements (e.g., tilting the head
upward [i.e., chin upward] or forward).
7. Patients may overestimate the duration of single
attacks and mild, residual symptoms after an at-
tack occasionally last minutes or hours. Further-
more, attacks may be triggered repetitively, caus-
ing more extended symptoms. The duration of
vertigo should not, however, generally exceed 1
minute; single attacks lasting consistently longer
should be considered atypical and spark consid-
eration of alternate or additional diagnoses.
8. Therapeutic positional maneuvers in canalolithi-
asis of the anterior canal have been reported as
effective [22,81]. Thus, if positional nystagmus
disappears immediately after positional therapy,
this strongly supports the diagnosis (see note 1).
Transition to canalolithiasis of the posterior canal
(2.1), canalolithiasis of the horizontal canal (2.2)
or cupulolithiasis of the horizontal canal (2.3), ei-
ther spontaneously or during positional maneu-
vers, also strongly supports the diagnosis.
9. The latency between the completion of the diag-
nostic positional maneuver and the onset of po-
sitional nystagmus may be as long as 30 seconds
in rare cases [20,57].
10. The positional nystagmus may have a small tor-
sional component, beating with the upper pole of
the eye toward the affected ear [2].
11. History and physical and neurological exami-
nations do not suggest another vestibular disor-
der or such a disorder is considered but ruled
out by appropriate investigations or such disor-
der is present as a comorbid condition that can
be clearly differentiated. As positional downbeat-
ing nystagmus also occurs as a sign of central
vestibular dysfunction, it is mandatory to exclude
CNS disease if positional nystagmus does not
cease promptly after therapeutic maneuvers.
113
Comments
Canalolithiasis of the anterior canal is rare compared
to posterior and horizontal canal variants [38,60,81].
This is probably related to the anatomical orientation
of the anterior canal, which allows particles to leave
the canal simply after lying down and sitting up again.
Positional nystagmus can be provoked in the supine
position with the head hanging straight below the
earth-horizontal and by Dix-Hallpike positioning, that,
no matter to which side the head is turned, stimu-
lates particle migration within the affected anterior
canal [2,6,16]. In the Dix-Hallpike position, nystag-
mus may be stronger or exclusively present with the
affected ear up or down. The most sensitive diagnos-
tic test for BPPV of the anterior canal seems to be
the straight head-hanging position [20,22]. Thus, in
canalolithiasis of the anterior canal, the direction of
the torsional component, rather than the side of the
Dix-Hallpike maneuver, indicates the affected side.
However, the small torsional component of the posi-
tional nystagmus can be easily missed in clinical prac-
tice, rendering identification of the affected side unreli-
able [2,6]. Identification of the torsional component of
nystagmus may be facilitated by eye movement record-
ing with video-oculography [16,22] or search-coils [2].
Attenuation of positional nystagmus with repeated
positional maneuvers (fatigability) may be supportive
of the diagnosis of canalolithiasis of the anterior canal,
but it is not present in all patients [20,57].
Transient downbeating positional nystagmus can
also occasionally be observed after treatment of BPPV
of the posterior canal, when the Dix-Hallpike maneu-
ver is performed. This finding may be due to translo-
cation of otoconia into the anterior canal or to otoconia
that have not left the posterior canal completely dur-
ing therapeutic positional maneuvers, dropping back
into the canal during the Dix-Hallpike maneuver, and
thus inducing an inhibitory nystagmus that is down-
beating [75].
3.2. Cupulolithiasis of the posterior canal
(pc-BPPV-cu)
A. Recurrent attacks1,2 of positional vertigo or po-
sitional dizziness3,4,5 provoked by lying down or
turning over in the supine position6 .
B. Positional nystagmus7 elicited after a brief or
no latency by a half Dix-Hallpike maneuver8,
beating torsionally with the upper pole of the eye
to the lower ear and vertically upward (to the
forehead) and lasting > 1 min.
C. Not attributable to another disorder9.
114 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria
Notes:
1. The duration of an attack of positional vertigo is
usually less than 1 minute as patients tend to re-
turn the head into a position where vertigo and
nystagmus cease. However, the duration can be
longer when the head is kept in the provoking po-
sition.
2. Besides attacks of positional vertigo, patients
may have prolonged mild unsteadiness.
3. BPPV typically leads to positional vertigo but oc-
casionally patients may complain of positional
dizziness.
4. Other complaints during the attacks include ex-
ternal vertigo (the visual sense of environmen-
tal motion that often accompanies the internal
vestibular sense) [13], unsteadiness, and vege-
tative symptoms such as nausea, sweating, and
tachycardia.
5. Positional vertigo or dizziness must be distin-
guished from orthostatic symptoms present only
on arising but not with other positional trig-
gers [13].
6. Attacks may not only be provoked in bed but also
by other head movements (e.g., tilting the head
upward [i.e., chin upward] or forward).
7. If positional nystagmus disappears immediately
after positional therapy, this further supports the
diagnosis.
8. A half Dix-Hallpike maneuver is performed
with the head turned 45 toward the side to be
tested and resting slightly raised from supine
(about 30 in flexion). This position is best suited
to bring the affected cupula to an earth-horizontal
position to be maximally deflected by the gravi-
tational force [29].
9. History and physical and neurological examina-
tions do not suggest another vestibular disorder
or such a disorder is considered but ruled out
by appropriate investigations or such disorder
is present as a comorbid condition that can be
clearly differentiated.
Comments
Cupulolithiasis of the posterior canal has rarely been
described [43]. Positional nystagmus may disappear
when the head is further reclined in the Dix-Hallpike
position [43]. A reversed Dix-Hallpike maneuver
with the head bent forward 90 from the upright posi-
tion after being turned 45 to the affected side may re-
veal nystagmus beating in the opposite direction com-
pared to the half Dix-Hallpike maneuver [29].
3.3. Lithiasis of multiple canals (mc-BPPV)
A. Recurrent attacks1 of positional vertigo or posi-
tional dizziness2,3,4 provoked by lying down or
turning over in the supine position5 .
B. Duration of attacks < 1 min6,7 .
C. Positional nystagmus8,9 compatible with canalo-
lithiasis of more than one canal during the Dix-
Hallpike maneuver and the supine roll test.
D. Not attributable to another disorder10.
Notes:
1. Besides attacks of positional vertigo, patients
may have prolonged mild unsteadiness.
2. BPPV typically leads to positional vertigo but oc-
casionally patients may complain of positional
dizziness.
3. Other complaints during the attacks include ex-
ternal vertigo (the visual sense of environmen-
tal motion that often accompanies the internal
vestibular sense) [13], unsteadiness, and vege-
tative symptoms such as nausea, sweating, and
tachycardia.
4. Positional vertigo or dizziness must be distin-
guished from orthostatic symptoms present only
on arising but not with other positional trig-
gers [13].
5. Attacks may not only be provoked in bed but also
by other head movements (e.g., tilting the head
upward [i.e., chin upward] or forward).
6. This criterion is not required when the labyrinth
is affected by cupulolithiasis.
7. Patients may overestimate the duration of sin-
gle attacks and mild, residual symptoms after an
attack occasionally last minutes or hours. Fur-
thermore, attacks may be triggered repetitively,
causing more extended symptoms. The dura-
tion of vertigo should not, however, generally
exceed 1 minute; single attacks lasting consis-
tently longer should be considered atypical and
spark consideration of alternate or additional di-
agnoses.
8. If positional nystagmus disappears immediately
after positional therapy, this further supports the
diagnosis.
 M. von Brevern et al. / Benign paroxysmal positional vertigo: Diagnostic criteria
9. The most frequent combination is a canalolithi-
asis of the posterior and horizontal canal of
one labyrinth. This may result in a transient
positional nystagmus with horizontal and tor-
sional components of equal intensity in the Dix-
Hallpike maneuver [2]. Alternatively, a mixed
torsional-vertical positional nystagmus compati-
ble with excitation of the posterior canal in the
Dix-Hallpike maneuver on one side and a pre-
dominantly horizontal positional nystagmus in
the supine roll test to both sides may be observed
in the same session [8]. Other combinations of
lithiasis of multiple canals may also occur but are
rarer.
10. History and physical and neurological examina-
tions do not suggest another vestibular disorder
or such a disorder is considered but ruled out
by appropriate investigations or such disorder
is present as a comorbid condition that can be
clearly differentiated.
Comments
Lithiasis of multiple canals is probably common, af-
fecting up to 20% of patients with BPPV [56,60]. Lithi-
asis of multiple canals probably occurs most often after
head trauma [8].
3.4. Possible benign paroxysmal positional vertigo
A. Attacks of positional vertigo missing one of the
criteria of a disorder coded above.
B. Not attributable to another disorder1 .
Notes:
1. History and physical and neurological examina-
tions do not suggest another vestibular disorder
or such a disorder is considered but ruled out
by appropriate investigations or such disorder
is present as a comorbid condition that can be
clearly differentiated.
Comments
This category may include e.g. (i) patients with posi-
tional vertigo without observable positional nystagmus
despite eye movement recording or with atypical po-
115
sitional nystagmus that nonetheless ceases after thera-
peutic positioning, (ii) patients with presumed involve-
ment of multiple semicircular canals that cannot be
specified, (iii) patients with simultaneous occurrence
of peripheral and central positional nystagmus [7].
Do not code as 3.4. possible benign paroxysmal po-
sitional vertigo if the patient fulfills the criteria for 1.4.
probable benign paroxysmal positional vertigo, spon-
taneously resolved.
Acknowledgements
This work was supported by travelling grants from
the Brny Society and from Neuro+ Berlin, a non-
profit association for neurological research. We thank
the Japan Society of Equilibrium Research, the Amer-
ican Neurotology Society and the members of the
Brny Society for valuable suggestions. Michael von
Brevern wishes to thank Alexandre Bisdorff and
Thomas Lempert for many fruitful discussions on the
classification of BPPV.
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